Elevated soluble E-cadherin during the epithelial-mesenchymal transition process and as a diagnostic marker in colorectal cancer

Zhu, Shuzhen; Zhao, Guanghui; Zhao, Xiangen; Zhan, Xi; Cai, Mei-Juan; Chen, Geng; Qian, Pu; Zhao, Qianqian; Fu, Qingsong; Huang, Chen; Wang, Qian

doi:10.1016/j.gene.2020.144899

Cited by 11 publications

(13 citation statements)

References 43 publications

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“…The result of this study was the expression of serum sE-cadherin level that was increased in the CRC cell which already undergone EMT. This result was different compared with usual research that expression of E-cadherin will decrease in the CRC with EMT process [26]. In this study, a correlation test between β-catenin cytoplasm expression and E-cadherin and N-cadherin was also conducted.…”

Section: Figure 4: the Intensity Of E-cadherin And N-cadherin Expressionsmentioning

confidence: 63%

Differences in the Expression of β-Catenin Nucleus/Cytoplasm Ratio e-Cadherin and n-Cadherin and Correlation of β-Catenin Cytoplasm and Cadherin in Model of Duke D Stage Colorectal Cancer Cell Line

Winarko

Rahayu

Soeatmadji

et al. 2021

Open Access Maced J Med Sci

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BACKGROUND: β-catenin has a critical role in the homeostasis processes. Wnt/β-catenin signaling mainly involved in the modulation of cancer cell development. AIM: This research aimed to investigate the differences of β-catenin expression observed in the form of nucleus–cytoplasm ratio, the differences of E-cadherin and N-cadherin expressions, and the correlation between N-cadherin and E-cadherin and β-catenin cytoplasm in Dukes D stage colorectal cancer (CRC), which is an advanced stage and has experienced metastasis. MATERIALS AND METHODS: This study followed an experimental research design. The processes of culture manufacturing and subculture preparation of Dukes D stage CRC cell line model were performed before the administration of β-catenin, E-cadherin, and N-cadherin antibodies. The next process was staining using fluorescein-5-isothiocyanate and rhodamine, and observations were performed using a confocal microscope. The number of cells was counted, and the intensity of antibody expression based on the arbitrary unit was measured. RESULTS: There was a significant difference between the expression of β-catenin nucleus and cytoplasm expression (p = 0.00), as well as between E-cadherin expression and N-cadherin expression (p = 0.00). In addition, a correlation also existed between an increased N-cadherin expression and decreased E-cadherin expression and β-catenin cytoplasm in Dukes D stage CRC, but the results were not significant (p = 0.837 and p = 0.108). CONCLUSION: In advanced-stage CRC (Dukes D), the Wnt signaling proved to be active and was characterized by a high expression of β-catenin nucleus, it activates the target gene. Similarly, at the Dukes D stage, N-cadherin expression increased whereas E-cadherin expression decreased in which causing the translocation of β-catenin into the nucleus.

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Section: Figure 4: the Intensity Of E-cadherin And N-cadherin Expressionsmentioning

confidence: 63%

Differences in the Expression of β-Catenin Nucleus/Cytoplasm Ratio e-Cadherin and n-Cadherin and Correlation of β-Catenin Cytoplasm and Cadherin in Model of Duke D Stage Colorectal Cancer Cell Line

Winarko

Rahayu

Soeatmadji

et al. 2021

Open Access Maced J Med Sci

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“…The difference between groups in terms of maternal age was statistically insignificant (p = 0.117, Mann-Whitney U-test). The median gestational week of delivery was 37 (range [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42] in the study group compared to 40 (range [38][39][40][41][42] in the control group and significantly differed between groups (p < 0.001, Mann-Whitney U-test). Median birth weight was 2160 g in the study group and 3475 g in the control group (p < 0.001, Mann-Whitney U-test).…”

Section: Basic Characteristics Of the Study And Control Groupsmentioning

confidence: 83%

Loss of E-Cadherin Staining Continuity in the Trophoblastic Basal Membrane Correlates with Increased Resistance in Uterine Arteries and Proteinuria in Patients with Pregnancy-Induced Hypertension

Pęksa

Kamieniecki

Gabrych

et al. 2022

JCM

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Pregnancy-induced hypertension (PIH), especially when complicated with pre-eclampsia (PE), could be a life-threatening complication of pregnancy. Pre-eclampsia is one of the leading causes of perinatal morbidity and mortality in women. Pre-eclampsia is mainly characterized by hypertension and kidney damage with proteinuria. Abnormal placentation and altered structure of the placental barrier are believed to participate in the pathogenesis of pregnancy-induced hypertension, leading to PE. In the current study, we aimed to analyze the immunohistochemical expression pattern of E-cadherin and p120, two markers of epithelial–mesenchymal transition, in placental samples derived from a group of 55 patients with pregnancy-induced hypertension, including pre-eclampsia and 37 healthy pregnant controls. The results were correlated with the presence of an obtained early uterine artery flow notching during diastole on Doppler ultrasound. We observed a higher frequency of discontinuous E-cadherin staining in the basement membrane of syncytiotrophoblast in patients with PIH/PE compared to controls (p < 0.001, Fisher’s exact test). Moreover, the loss of continuity of E-cadherin expression correlated with the presence of a bilateral early diastolic notch on Doppler ultrasound (p < 0.001, Fisher’s exact test) and the presence of proteinuria (p = 0.013, Fisher’s exact test). These findings suggest that E-cadherin contributes to the integrity of the placental barrier, and its loss could be an immunohistochemical marker of PE.

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“…A correlation between sE-cadherin level and metastatic dissemination has also been noted by others. Serum concentration of sE-cadherin increased during colorectal cancer metastasis in mice and in patients with late-stage cancer [12,16]. Furthermore, elevated sE-cadherin levels have been significantly associated with hepatic metastasis and muscle invasive bladder cancer [17,18].…”

Section: Discussionmentioning

confidence: 99%

“…Identifying critical hubs of tumor molecular machinery is essential in developing efficacious cancer treatment options. Since the serum concentration of sE-cadherin has been reported to be upregulated in patients with several cancers including PCa [7,8,12,13], we aimed to explore the impact of sE-cadherin on PCa cell growth and invasive behavior.…”

Section: Discussionmentioning

confidence: 99%

Deciphering the Molecular Machinery—Influence of sE-Cadherin on Tumorigenic Traits of Prostate Cancer Cells

Tsaur¹,

Thomas²,

Juengel³

et al. 2021

Biology

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The serum level of soluble (s)E-cadherin is elevated in several malignancies, including prostate cancer (PCa). This study was designed to investigate the effects of sE-cadherin on the behavior of PCa cells in vitro, with the aim of identifying a potential therapeutic target. Growth as well as adhesive and motile behavior were evaluated in PC3, DU-145, and LNCaP cells. Flow cytometry was used to assess cell cycle phases and the surface expression of CD44 variants as well as α and β integrins. Confocal microscopy was utilized to visualize the distribution of CD44 variants within the cells. Western blot was applied to investigate expression of α3 and β1 integrins as well as cytoskeletal and adhesion proteins. Cell growth was significantly inhibited after exposure to 5 µg/mL sE-cadherin and was accompanied by a G0/G1-phase arrest. Adhesion of cells to collagen and fibronectin was mitigated, while motility was augmented. CD44v4, v5, and v7 expression was elevated while α3 and β1 integrins were attenuated. Blocking integrin α3 reduced cell growth and adhesion to collagen but increased motility. sE-cadherin therefore appears to foster invasive tumor cell behavior, and targeting it might serve as a novel and innovative concept to treat advanced PCa.

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Elevated soluble E-cadherin during the epithelial-mesenchymal transition process and as a diagnostic marker in colorectal cancer

Cited by 11 publications

References 43 publications

Differences in the Expression of β-Catenin Nucleus/Cytoplasm Ratio e-Cadherin and n-Cadherin and Correlation of β-Catenin Cytoplasm and Cadherin in Model of Duke D Stage Colorectal Cancer Cell Line

Differences in the Expression of β-Catenin Nucleus/Cytoplasm Ratio e-Cadherin and n-Cadherin and Correlation of β-Catenin Cytoplasm and Cadherin in Model of Duke D Stage Colorectal Cancer Cell Line

Loss of E-Cadherin Staining Continuity in the Trophoblastic Basal Membrane Correlates with Increased Resistance in Uterine Arteries and Proteinuria in Patients with Pregnancy-Induced Hypertension

Deciphering the Molecular Machinery—Influence of sE-Cadherin on Tumorigenic Traits of Prostate Cancer Cells

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